CM heme/onc Flashcards
what are four things that anemia can come from?
- excessive blood loss
- destruction (hemolysis) of RBC
- deficient RBC production because of nuitritional elements
- bone marrow failure
polycythemia
increase in red blood cell count
erythropoietin
hormone that increases production of RBC in response to decreases O2 levels in the tissues, released by the kidneys
erythrocyte characteristics
mature RBC, biconcave disk, no nucleus
what does sideroblastic anemia mean?
term for the failed synthesis of RBC (bone marrow not working correctly)
(thalessemia, sickle cell, idiopathic)
RBC count test
measures the total # of RBC in microliter of blood
percentage of reticulocytes (immature RBC)
an index of the rate of red blood cell production
hematocrit test
percent of RBC in blood by volume. (spin down the reb and divide volume by total volume plus serum)
mean corpuscular volume, MCV
size of RBC, average volume size of the RBC
microcytic, macrocytic, normocytic
mean corpuscular hemoglobin concentration MCHC
concentration of hemoglobin in EACH cell
color of hemoglobin terms
normochromic, hypochromic, hyperchromic
mean cell hemoglobin (MCH)
average hemoglobin weight/mass in each cell
CBC test
includes:
counts: number of red blood cells
hemoglobin: measure of the functional portion of RBC, weight
hematocrit: percent of RBC in blood by volume
MVC: mean cell volume, average size of rbc
MCH: hem
what is anemia? what does this result in?
abnormall low number of circulating RBCs or low concentration of hemoglobin
results in tissue hypoxia
what two things account for half of the anemia found worldwide?
parsitic/infectious disease
what are 5 red blood cell functions?
1. transport oxygen
- transport CO2
- acid/base metabolism
- maintain viscosity/vascular tone
- plug clots in addition to platelets
what are three main things you do to increase O2 delivery by RBC?
- increase blood flow or Q (stands for blood flow)
- increase red cell mass or hemoglobin
- increase O2 extraction
if the body is trying to increase blood flow or Q in response to oxygen demand, what 2 things would you see?
1. increase cardiac output
(HR, pressure, murmers, bruits, tinnitis)
2. changes in tissue perforation
(shunt blood from skin and kidney to rain, heart, and muscle, this is why you get pale!, increases erthropoeitin)
if the body is trying to increase the red cell mass, what would you see?
what happens of the EPO is really high?
what happens to the viscosity of the blood?
Kidneys->EPO->marrow erythropoiesis->reticulocytosis and increase #RBC
this accound for growing pains
- if EPO really high can stimulated maturity outside of the BM*
- this increases viscosity of the blood*
explain what the body does in oxygen extraction to increase the oxygen profusion into the tissues? which way does the curve shift?
2,3-diphosphoglycerate (2,3-DPG) binds to hemoglobin and decreases hgb affinity for oxygen, this causes it to be released into the tissues
“makes it harder for oxygen to stay attacked to hgb”
shifts dissociation curve to the right
what is the gold standard for anemia detection?
Red blood cell count
(difficult to do)
what is the definition of anemia according to the WHO?
hb<12.5 gm/dl
what concentration of hemoglobin are people typically symptomatic? what concentration is considered the be anemia?
anemic: 12.5 gm/dl
symptomatic: 10gm/dl
what is the first thing you should look at when addressing anemia? what percentage of these are normal in the blood? how much larger are these than regular RBC? what do you see in them that is different then regular RBC?
reticulocyte count
normal: .5-2.5% of RBC are reticulocytes (10% larger than red blood cells)
reticular network of RNA
explain the MCV values that are associated with microcytic, normocytic, and macrocytic RBC?
microcytic: <80
normocytic: 80-100
macrocytic: >100
what two anemias would you see microcytic RBC?
Fe deficiency
sideroblastic lead poisoning
in decreased RBC production you get:
low reticulocyte, normocytic RBC
low reticulocyte, macrocytic RBC
what 4 conditions would you see in the first? and what 3 conditions would you see in the second?
low reiculocyte count and normocytic
- anemia of chronic disease
- bone marrow failure
- RBC aplasia
- low erythropoeitin (renal failure)
low reticulocyte, macrocytic
- B12 deficiency
- folate deficiency
- hypothyroidism
if normal to elevated reticuloctye, and normocytic
…..
what two categories does this indicate? what are four conditions in the second category?
- hemmorage
- hemolysis
(G6PD, sepsis, ABO incompatability, spherocytosis)
if normal to increased reticulocyte, and microcytic this means…
hemoglobinopathies
what is iron essential for?
developing bactericidal free radicals in neutrophils
what is the most common anemia in the world? what causes it?
what about in america?
iron deficient anemia!!
MOSTLY FROM PARASITES!! GROSS
In america: menses
Iron Deficient Anemia
what size and color? what two unique characteristics about this cell type hint: shape? what are 3 main causes? what should you always suspect? what are 5 unique presentations you might see on PE? what is the treatment? for how long?
hypochromic, microcytic anemia (since no iron to give shape or color)
anisocytosis (unequal size) and piokilocytosis (tear drop shapped)
common causes: blood loss (menses, occult from colon, esophagus, stomach), pregnancy, vegan diet
**always suspect malignancy**
pica (eating dirt/paint), cheilosis, koilonchia “spoon nails”, glottitis “smooth tongue”, esophageal webs, pallor, tachycardia
treatment: Ferrous sulfate 325 mg 3x a day, vitamin C to make absorb better and uptitrate, OR GLUCONATE which is IM or IV
TREAT FOR 6 MONTHS!!
what can cause blood loss in iron deficient anemia? 4 things
GI blood loss from NSAIDS, PUD, cancer
blood donation
trauma
menses
where is iron absorbed? where is it stored? how is it transported?
absorbed: duodenum and jejunum bound as transferrin
stored: mostly in liver, spleen, and bone
what would you see on the labs for iron deficient anemia?
5 things!
- Low Iron <50
- High TIBC (since none to bind, very avaliable)
- low ferritin (since none to store)
- low reticulocyte
- hypochromic, microcytic cells
if a woman is pregnant….does iron deficient anemia effect the baby?
YES!!
what is the number one cause of iron deficient anemia? what are 3 other causes?
- blood loss! need to find the cause!!
2. malignancy! need to think about this
- dietary, vegan!! less common
- poor iron absorption/ trauma
sideroblastic anemia (lead poisoning)
what are the size of the cells? reticulocyte count? platelets? what are three unique lab results you will see with lab testing? what will the patient present with for symptoms? what do you do for treatment depending on the levels of lead in the blood? what does the location of the lead tell you about how long it has been in the body? what does the bone marrow produce?
microcytic, decreased reticulocytes, low platelets
basophilic stippling, elevated lead, erythrocyte protoporphyrin, bone produces ringed sideroblasts instead of health RBC
PE: lead on the gum lines, vomiting, abdominal pain
high serum levels: acute attack
if in the bone: hard to tell how long its been there
BLL>20, medical and environmental intervention
BLL>45, chelation
what do you need to caution for in children with lead poisoning aka sideroblast anemia? what happens in this?
reduced hemoglobin synthesis cause iron accumulation esp in mitochondria
watch for neurological symptoms in children
Vitamin B12 deficient anemia
what size and color at these RBC? what factor sets this appart from folate deficient anemia and what are the 5 presentations? what are the 6 things that can cause this and where are the two general sections of the GI system that are effected? what are the 4 important lab results that point to this?
macrocytic/megloblastic anemia, normochromic
can occur from vegan diet, bariatric gastric surgery (MOST COMMON WAY TODAY), ilium resection, chrons disease, pernicious anemia (no intrinsic factor), gastritics
neurologic symptoms, stocking glove paresthesia, loss of position, vibratory sense, balance, glottitis
On lab exams find:
1. antibodies for intrinsic factor
2. MCV >103
2. serum b12 low
4. multinucleated neutrophils!!! 5-6 lobes
Tx: oral supplement or cyanocobalamin nasal spray
explain how B12 is absorbed and which conditions effect these stages?
B12 is bound to intrinsic factor that prevents it from being absorbed until it reached the ilieum
chrons disease, ilium ressection effect: where it is absorbed
gastric surgery, pernicious anemia, gastritis effect: where intrinsic factor is made
***both of these cause B12 deficiency either in its protection or its absorption!***
what cells produce intrinsic factor that are important for the absorption of B12? where are they located?
parietal cells in the stomach
gastritis PUD can prevent this from working
no intrinsic factor, no absorption
what are three things can cause poor absorption of B12 for anemia?
alcoholism
fish tapeworm
elevated LDH
what are the 3 treatment options for B12 deficient anemia?
- life long vitamin B supplement IM monthly (1000 ug)
2. cyanocobalasmin nasal spray
***neuro symptoms are reversible if treated within 6 months***
explain the schillings test and what it tells you?
tells you which there is a B12 deficiency
if pernicious anemia where no intrinsic factor: no b12 in blood
if give intrinsic factor and see B12 in the urine then: pernicious anemia
if no B12 in the uring after intrinsic factor then: problem with absorption in illium, not intrinsic factor
G6PD deficient anemia
what genetic link is this connected with? what two populations of people is this common in? what size are the cells? what is one unique presentation do you see? exposure to what 3 things can cause this? what are the 5 things you will see on the lab results? how is it treated?
x-linked recessive, african america males (12%), or greeks/mediteranean (20-30%)
normocytic anemia, increased risk of HEMOLYSIS UNDER STRESS,jaundice
G6PD protects RBC agains oxidative stress that can damage the RBC beyond repair
fava beans
infection
oxidative drugs
heinz bodies, low G6PD, bite cells, increased reticulocytes and serum bilirubin
Tx: self limiting, when the the stressor is resolved then normal RBC produced again
what are the 5 drugs and 1 infection that can cause oxidative stress for someone with a G6PD deficiency?
- aspirin
- FAVA BEANS
- sulfa drugs
- quinidine
- antimalarials
condition: hepatitis
what are people with G6PD deficient anemia at increased risk to get?
DMT2 since buildup of unused glucose
IDK WHY! just does?!
hemmoragic anemia
what do you see initially? after 1 week? and in extreme cases or long bleeding what would you see in iron panel?
initially: normochromic normocytic
1 week: increase in young RBC and reticulocytes
if significant hemmorage or decreased iron stores: decreased Fe, increased TIBC, decreased ferritin
hemoglobin synthesis is critcally dependent on….
IRON!! needed to make it in the bone marrow
sickle cell anemia
what is the inhertiance pattern? what is the difference between heterozygous/homozygous? when do the problems first occur? where is the mutation? what are 8 things that can prompt sickeling? what are 7 presentations you can see with this disorder?
autosomal recessive
heterozygous 1 Hb S gene: 40%
homozygous 2 Hb SS gene: 80-95%
problems start about 6 months after birth during transition from Hb-F to Hb
mutation in B chain, cause it to sickle under/from:
dehydration, hypoxia, acidosis, infection, temp changes, exertion, alcohol, medical procedures
causes acute painful syndrome, acute chest syndrome, splenic sequestration, aplastic crisis, hemolytic crisis, hand foot disease, “silent” cerebral infarction (35%, subtle but permanent)
what is this and what condition do you commonly see this with?
hand and foot syndrome seen with sickle cell
commonly the first presentation
soft tissue swelling with new bone formation and moth eaten lytic process at proximal aspect of fourth phalanx
no leukocytosis or erythema with the swelling
what is the goal for the Hb and HbSS for patients with sickle cell?
Hb>10%
HbSS <30%
helps to determine when transfusion or intervention are required
explain the pathphys of sickle cell
increased RBC destruction
inability to maintain hemoglobin
sickling of cells=increased blood viscosity and ostruction
MORE FRAGIL=hemolysis!
what is the life expectancy for a pt with sickle cell?
40-50 years
die young from infections
Explain actute painful crisis and acute chest syndrome seen in sickle cell pts
acute painful crisis:
excrutiating, can occur anywhere
acute causes vasco occlusion and ishchemia
acute chest syndrome
25% of deaths!
respiratory distress
explain aplastic crisis seen in sickle cell and the five things that can cause it?
stop of RBC production, and since their RBC live so much short ~20 days, they get EXTREME drop in hemoglobin causing aplastic crisis
parvarovirus B19, infection, bone marrow toxins HPV, folic acid deficiency
explain the hemolytic crisis seen in sickle cell and what patients with another disease is this commongly seen with? what two things can prompt this?
higher rate of hemolysis than normal
frequently in patient with G6PD deficient
actute bacterial infection/oxidatative drugs
what do sickle cell patients need to avoid?
altitiudes over 7,000 feet and deep sea diving!
induces sickling
what do you see for lab results for a patient with sickle cell? 6 things!!
- howell jolly bodies
2. Hgb S >50%
3. hb 6-8
4. RBC last 10-20 days
- high reticulocytes
- high ferritin/serum bilirubin
what treatment options are avaliable for someone with sickle cell?
- hydration
- pain meds!!
- transfusion
- folate supplementation
- iron chelation if Fe overload
- preventative vaccines for S. pneumonia, H. influenzae
-prophylatic penicillin from birth to 6 years
hydroxyurea
explain hydroxyurea for sickle cell patients 3 things
- Decrease DNA synthesis
- Inhibit sickling
- Increase Hb F inhibits Hb sickling
**prevents complications and increases life span**
what are sickle cell patients are increased risk for?
(6 things)
- infection with encapsulated organisms
- aseptic necrosis
- CVA
- chronic leg ulcers
- splenic infarc THESE PATIENTS ARE ASPLENIC (DON’T HAVE A SPLEEN THAT WORKS WELL SO NEED TO MAKE SURE THEY ARE VACCINATED ESP AGAINST STREP PNEUMONIA
- retinopathy
explain HbSC and HbSS in sickle cell
Hb SC is the trait for sickle cell, heterozygous and range of symptoms vary
Hb SS the disease for sickle cell, homozygous, severe disease
anemia of chronic disease
what three cytokines are released? this causes what 3 things to decrease? what 2 things to increase? what 8 things can cause it? what 3 lab results are important? what do you do to treat it?
chronic inflammation and activation of IL1, IL6 and TNF
leads to decrease of EPO, transferrin synthesis, GI absorption
increased iron storage/ferritin, increase iron storage in macrophages
osteomyelitis, endocarditis, TB, HIV, malignancy, autoimmune (RA, SLE), IBS, Renal failure
ferritin elevated (since body storing it), TIBC decreased (since stored not circulating), low iron
Tx: treat underlying condition, it will go away
beta thalaseemia
what chain is effected in this? what parts of the world is this common in? what unique cell do you see in the lab results? what are the two main classifications of B thalaseemia? when is the more severe on diagnosed? what are four clincial presentations of this? what are 3 treatment options? what do you want to keep [hb] at? what test do you use to tell the difference between Fe and thallessemia?
deficient synthesis of B-globin chain of hemeoglobin
(results in increase A) African/mediteranneans
HEINZ BODY CELLS!! “Target cells” “HAIR ON END APPEARANCE ON XRAY”, FRONTAL BOSSING
minor: heterozygous, sufficient Hb sythesis
major: homozygous! SEVERE transfusion dependent anemia, diagnosed 1st year of life when hb F turns to Hb A (adult) “cooleys anemia”
growth retardation, hepatosplenomegaly, abnormal facial formation, fractures/osteopenia, delayed or absent puberty, hypogonadism
Tx: regular blood transfusions to keep hemoglobin at 12 mg/dl, avoid Fe supplements, bone marrow transplant/splenectomy
MENTZER INDEX
which one is more severe B thalmassemia or A thalmessmia?
B thalmassemia because the accumulation of A chains is more toxic
how are the thalassemias named?
what are the general treatments listed by professor? (4 treatments)
FOR WHAT THEY ARE DEFICIENT IN!!!
1. blood transfusion with chelation
2. hydroxyurea (increases HbF)
3. bone marrow transplant
4. splenectomy
xalpha thalessemia
what are the deficient in? what type of cells can be present? what nationality of people are most common? explain the four stages? size and color? what lab results remain normal? what do you treat with? what should you avoid?
deficient a-globin chain, 4 stages target cells Heinz bodies!!
ASIANS
usually diagnosed if iron supplemets for suspected iron deficient don’t work
- silent carrier, 1 gene deleted
- trait, 2 gene deleted leading to mild hemolytic anemia
- Hb “H”, 3 genes deleted, hemolytic anemia without transfusion need
- lethal at birth, hydrops (seen in pic)
microcytic hypchromic but not very anemia, normal iron, TIBC, ferritin
Tx: folic acid supplement, avoid iron, if that doesn’t work then transfusion but not dependent like B thalassemia
aplastic anemia
what is this? exposure to what 6 things can cause this? what are the two age groups? what are the symptoms? what are the two treatments?
hypoproliferative anemia, low marrow activity decreased RBC, WBC, and platelets
“panocytopenia”
unknown cause but can be from radiation, chemo, toxins, meds, autoimmune, tumors of thymus
Biphasic: 12-25 and 60+
PE: insidious onset, mucosal hemmorage, mennorhasia, epitaxis (lots of bleeding since less RBC), palpations, systolic ejection
TX: stem cell replacement bone marrow 75% survive
in those that don’t qualify chemo therapy remission in 50% of people
folate deficiency
what is the most common cause of this? what are four things that can cause this? what size are the cells? what two things do you see on the labs? what 5 drugs can cause this? what is the treatment?
most often caused by poor dietary intake, low fruits and veggies
absorbed in the ileum
macrocytic, hypersegmented PMN, folate <150
alcoholics, defective absorption (chrons, ulcerative collitis), pregnancy, folic acid antagonist drugs
drugs: methotrexate, alcohol, phenytoin, trimethoprim-sulfamethozole, sulfasalazine
tx: 1 mg folic acid a day
spherocytosis
who is it common in? what test should you do? what can you often get with this? what is the treatment?
congenital, Northern europeans
RBC shaped like spheres, causing premature hemolysis
COOMBS test! it is autoimmune, checks for these antibodies
gallstones
splenectomy cures it but doesn’t help abnormal shape since the spleen gets rid of the abnormally shapped cells. taking this out allows the cells to live longer.
osmosity fragility test gold standard?! (wikki)
what are the 5 stages of hemostasis? (stoppage of blow flow)
- vessel spasm
- formation of platelet plug
- blood coagulation and development of insoluable fibrin clot
- clot retraction
- clot dissolution
prothrombin time (PT) test
used to monitor warfarin, test liver funciton, and vitamin k definiceny
TESTS extrinsic pathway
factor VII first to drop
partial prothrombin time (PTT) tests
how long it take the blood to clot from the intrinsic pathway
used to monitor the effectivness of heparin!!
explain why PT and PTT are usually run together?
they both share the same final pathway so by only running one you can’t tell which one it is, if its before or at the shared part
when is the intrinsic clotting pathway initiated
damage to the inside of the blood vessel
when is the extrinsic pathway activated for clotting?
tissue damage
PT-INR test, when do you start to worry about bleeding?
standardizes the PT across different labs
1= normal
4.5=worry about bleeding
used to monitor bleeding
thrombin time test
thrombin is the enzyme that converts fibrinogen to fibrin in the last step of coagulation, estimates the rate of formation of fibrin
mix patient plasma with commercially supplied thrombin and measures clot time
also tests presence of heparin/fibrinolysis
what are normal levels of platelets?
what level do you worry about bleeding?
what level do you worry about spontaneous bleeding?
normal platelets: 150,000-450,000
risk of bleeding <50,000
danger zone, risk of spontaneous hemmorage <10,000
what/when do thrombocytopenia purpuras develope?
big bruising from low platelets
what are three important parts that help prevent agains abnormal clotting?
protein C, S, antithrombin II
these make the fibrolytic system
if one of these aren’t there you get abnormal clotting!
breaks down clot after formation and prevents abnormal clotting, allows for wound repair and healing
coumadin
anticoagulant that interferes with vitamin k dependent factors
extrinsic=VII=PT=coumadin
heparin
increases antithrombin III
intrinsic=PTT= 12, 11, 9,8=heparin
what five drugs can cause thrombocytopenia?
sulfa, quinine, NSAIDS, heparin, penicillin
idiopathic thrombocytopenia purpura (ITP)
what happens in this? what are the two types and the characteristics of each (who, platelet #)? what are the two main causes of this? what is the treatment?
immune system destroys platelets
acute: self limited, autoimmune IgG diorder children 10,000-20,000, eosinphilia
chronic: any age, coexists with other autoimmune disease 25,000-75,000
autoimmune or VIRAL CAUSE IN CHILDREN!
post infection, HIV, Lupus, malignancies (MUST RULE THIS OUT!!!)
TX: glucocorticoids (steroids), IV Ig. splenectomy
thrombolic thrombocytopenia purpura (TTP)
what happens in this? what are four presentations this can take? two pain concepts behind this that it causes? what are four test results? what are thet two treatment options?
development of clots in microcirculation because of microvascular damage (this caused by pregnancy/autoimmune)
microangiopathic hemolytic anemia (intravascular hemolysis with consumptive thrombocytopenia)
microvascular occlusions cause widespread ischemia causing purpura, abdominal pain, neurologic symptoms because of hypoxia, and renal dysfunction
intravascular hemolysis (RBC get damanged trying to move through the clots and rupture) and consumptive thrombocytopena (all platelets used up in clotting)
testing: decreased platelets, hemoglobin, reticulocyte. increas in bilirubin (shows RBC lysis)
TX: plasma exchange transfusion, glucocorticoids
von willebrand thrombocyte
what type of genetic inheritance does this show? what happens in this? explain the 3 types? where do you see the bleeding? what are 4 lab findings (3 abnormal)? what pathway does this effect? what are the 2 treatment options?
deficient/defect in vWF, autosomal dominant
deficiency vWF: doesn’t stabalize factor VIII or allow platelets to stick to the vessel wall for clotting
prolongs bleeding time! RISTOCETIN ACTIVITY IS THE GOLD STANDARD TO TEST (ABX that tests coagulation in vitro)
type 1: most common, mild bleeding 75-80%
type 2: vWF abnormal
type 3: rare, most severe, low vWF and factor VIII
bleeding: nasal, sinus, vagina, GI, menses
LABS: LOW vWF, PT NORMAL, PFA (PLATELET FUNCTION ABNORMAL), PTT ABNORMAL SINCE EFFECTS THE INTRINSIC PATHWAY WITH FACTOR VIII
TX:
- Cryoprecipitate (plasma with vWF and VIII)-surgery/complications
- vaspressin DDAVP/vasopressin (stimulates release of vWF from endothelia cells)
in von willebrand thrombocyte, what can the decreased levels of Factor VIII lead to?
pseudohemophilia A
hemophilia A “classic”
what genetic heredity type is this? what happens in this? what do you need to differentiat it from and how do you do that? what are four clincial presentations and what is the key one? what 3 tests are improtant? what are the two treatment options?
deficiency of Factor VIII which is needed for clotting, x-linked recessive males
excessively long clotting time, most severe bleeding disorder
hemarthrosis (KEY!!), bleeding after circumcision, intracranial bleeding, compartment syndrome (increased pressure in arm/leg/confined space) epitaxis, bleeding into small tissues,
**include neuro bleeding and hemarthrosis/compartment syndrome**serious bleeding
factor VIII low, PTT prolonged, vWF normal(differentiates with von wilebrand), normal PT, PFA, fibrinogen, platelet count!!
TX: fresh prozen plasma, recombinant factors, prophylaxis with recombinant factor VIII, desmopression (increases VIII)
hemophilia B
“xmas disease”
what is the deficency here? what is the genetic hereditary? males or females? where are 3 common places to have bleeding? what are two important lab results? what are two treatment options?
deficiency of factor IX, x-linked recessive
MALES
hematomas, hemarthrosis, compartment syndrome but different factor than A!!
Factor IX low, PTT increased (since intrinsic pathway deficiency), platelet count normal
Tx: fresh frozen plasma, recombinant factors, prophylaxis with Factor IX, on demand factor replacement
disseminiated intravascular coagulation (DIC)
What generally happens in this? what are 6 things that can cause this? what are 3 important presentations of this? what are four important lab results you would see with this? what is the treatment and why is this so complicated?
widespread microthrombi, severe thrombocytopenia
clot then bleed to death, trigger usually surgical castastrophe or sepsis
thrombotic followed by consumptive and fibrinolytic process, everything is consumed, all the platelets and coagulation factors, clogs everything with fibrin deposition and clotting uses all the resources which makes you more apt to bleed in other places. this compromises tissue blood flow and leads to organ death
clotting and bleeding
occurs in: infection with gram negative sepsis endotoxins malaria, rocky mountain spotted fever, malignancies, trauma, pregancy and birth
Presentation: WIDESPREAD HEMMORAGE, RENAL FAILURE, GANGRENE, shock
LAB RESULTS: PROLONGED PT/PTT/INR SINCE EVERYTHING IS CONSUMED, ELEVATED D DIMER FROM INCREASED FIBRINOGEN DEGREDATION, DECREASED FIBRINOGEN, SCISTOCYTES SINCE RBC TRY TO SQUEEZE THROUGH THE CLOTS AND GET DAMAGED
Tx: treat underlying cause, Fresh frozen platelets if severe bleeding, **also need to treat the clots so this is VERY complicated!!!!***
what is the mortality from diffuse intravascular coagulation?
10-50%
how long can it take to detech a tumor clinically?
10 years or 30 doubling times
explain 6 characterists of malignant tumor cells
- little resemblance to original tissue and undifferentiated anaplasia
- lost ability to supress proliferation, mutate quickly
- do not do normal function
- no clear boundaries and infiltrate surround tissues
- metastasize by blood or lymph
- comrpess or destroy other tissue
explain the 3 order of events for a malignant tumor to form?
what four characteristics are under the last step?
1. metaplasia
2. dyplasia
3. ANAPLASIA
loss of morphological characteristics of mature cells
- nuclear pleomorphism
- nucleoli enlarged
- high proliferation index
- atypical mitosis
what are the four differences between malignant and benign neoplasms?
- characteristics of cells
- rate of growth
- local invasion
- ability to metastasize
tertoma
when do these usually occur? what does it resemble? what 3 things can it contain? is it benign..exception? where are the three locations typically to get them?
usually congenital
encapsulated tumor with tissue resembling normal derivates
can contain rudimentary organs, teeth, hair, bone
typically benign, except testicular teratomas in men
ovarian: pelvic pain, torsion
mediastinal: compression airways
sacrococcygeal: newborn (in pic)
what is the major cause of death in cancer? what are the three fashions this can take place?
metastasis by
- lymphatic-carcinomas, melanomas, can get to blood vasculature from thoracic duct
- hematogenous, typically follows venous drainage pattern
- transoelomic (peritoneal, pericardial, transthoracic, subarachnoid)
what are the four most common sites for metastasis?
lung, liver, bone, brain
what are the two cancer associated genes?
- protooncogenese: mutates normal gene that becomes an oncogene and has increased expression of growth factors, transcription factors ect… literally gene for cancer
2. tumor suppressor gene- genese that normally inhibit cell proliferation and protect against oncogenes
what are the three stages of tumor cell transformation?
- initiation- exposure of cells to carcinogenic agent and initial mutation occurs
2. promotion- mutated cells are stimulated to divide causing unregulated accelerated growth
3. progression tumor cells develop more mutations which make them more aggressive
what is a carcinoma in situ
early form of cancer
absence of invasion. not through basement membrane
not invading surrounding tissue
no potential for metastacies
burkitt’s lymphoma
(non hodgkins)
where is this an endemic? what type of cell is imporant to see here? what virus does this have a strong association with?
endemic in Africa
“starry sky”, abdominal fullness-cells contain lipid vacuoles!! KEY
EBV association
Type 1: African Jaw/face-100% with EBV associated with malaria
Type 2: sporadic abdomen/bone marrow; 20% EBV
Type 3: HIV associated 40% EBV lymph node/bone marrow
hodgkin’s lymphoma
what are four characteristic findings of this? what is this closely associated with? what two tests can you do? what are the two treatment options? what is the age group?
- reed sternburg cells “owl eyed”
- contigious spread, typically cervical, mediastinal, and supraclavicular first effected (moves to neighboring lymphnodes)
- pain after alcohol consumption
- pelbestein fevers (fluctuate over extended periods of time)
EBV association inf 50%
bimodal age group, peaks in 20s then again in 50s
DX: Ct abdomen/pelvix/chest or PET CT, BM biopsy
TX: radiation or chemo depending on the stage (described later)
explain the ANN arbor staging for lymphoma? how does this impact the treatment for hodgkins lymphoma?
if the staging for hodgkins lymphoma is 2a or above RADIATION!!!
2b and worse=ABVD CHEMO/ BEACOPP chemo!!!
(just FYI, this isn’t effected in non-hogkins lymphoma)
what are the four drugs included in ABVD chemotherapy for Hodgkins lymphoma? what side effects do you need to worry about?
Adriamycin
bleomycin
vinablastine
dacarbazine
mutiple myeloma
what is the pnuemonic associated with this cancer and what does each part mean? what cell is affected here? what are two important test results you will see? what are the two treatment options for this? what group of people is this most common in?
BREAK ACRONYM-malignany of plasma cell, more common in african american men
B: bone pain-lytic bone lesions, increased bone fractures particullary in back, spine, ribs
R: reccurent infections strep pneumoniae, gram neg encapsulated, non function Ig
E: elevated calcium since bone being destroyed
A: anemia (crowding out of bone marrow, overgrows RBC/platelets=less RBC)
K: kidney failure (increased Ig deposit in kidney, increased viscosity=kidney failure)
monoclonal Ig Spike, “M” protein spike, bence jones proteins in the urine,
TX:chemo, BM transplant (not commonly done since many patients elderly)
Acute lymphacitic leukemia (ALL)
what is this the most common of? what subsets of cells does it involve? what will you see on the smear? what condition is it associated with? what is one caution you NEED to address when treating this? what is used for diagnosis and what is the treatment?
1 cause of cancer in children!!
very young: 3-7 yrs
associated with down syndrome
T or B lymphblasts subsets
**hides in CNS so must treat with prophylaxis!
bone pain since ramped up
DX: smear, BM biopsy
TX: 3 phases of chemo!! prophylaxis chemo Ara-c for cancer hiding in CNS, LUMBAR PUNCTURE FOR CNS INVOLVEMENT!!!
explain the two T and B cell subsets of acute lymphocytic leukemia!!
what are the chromosomes that are effected in B cell ALL? what are the symptoms associated with T cell ALL?
This was from khan academy and meded
Acute myelogenous leukemia (AML)
who do you see this in? what are two important things you will see on the SMEAR? what percent achieve remission? what are the three treatment options? what exposure do you usually have to get this?
adults, acute picture
>20% blasts, AUER ROD CELLS, bone pain since ramping up cells
WBC>100,00
70% achieve remission
EXPOSURE: BENZO, CHEMO, RADIATION
TX: combination chemo, bone marrow transplant vit A
chronic lymphocytic leukemia (CLL)
who is this most common in? what type of cells are most common? what is important cell seen on slide? what are three other presentations of this? what do you do for treament of this for the 3 different pt groups? what do the symptoms come from? what is a halmark here?
elderly, asymptomic, die with it not from (3-10 years LE)
95% B cell derived!
B cell “smudge cells” (not structually strong since immature)
hypgammaglobinemia (don’t make as many since B cells messed up)
affects the bone marrow, liver, spleen, lymphnodes! gets bigger
in the lymph node starts a small lymphocytic lymphoma the transfors by richter transformation to diffuse B cell lymphoma (SOLID MASS)
causes autoimmune hemolytic anemia (nonfunctioing antibodies attack RBC, random, but imporant!)
acceptable to wait and watch in asymptomatic
usually come to the office for something else and are diagnosed on accidental findings
symptoms come from overcrowding->thrombocytopenia/anemia->beeding
>65 asymptomic: wait and watch
>65 symptomatic: chem
<65: stem cell treatment
TX: chlorambucil/fludarabine if chemo
chronic myelogenous leukemia (CML)
what two genes are associated wit this and which one is more specific? which line of cells can this be in and which is the most common? what are the three stages for this? what are the two treatment options? what kills these patients?
Adults
- philidelphia chromosome (95) 9/22
- BCR-ABL gene
- relies on tyrosine kinase inhibitor
- most common in neutrophils, but can be in ANY of the myeloid cell lines
- blast crisis which transforms it to acute myelogenous leukemia **this is what kills these patients**
WBC>100,000
Three stages:
- chronic: asymptomatic
- accelerated: start to see symtoms
- acute: blast crisis! >30% blast in the BM, then transforms to AML
TX: TYROSINE KINASE INHIBITOR IMATNIB (works on BCR-ABL), ALLOGENIC BONE MARROW OR STEM CELL TRANSPLANT
what are immature WBC’s called? if there is an increased number of these what does this cause? what three things should you think of when you see this?
“Band cells”
causes a shift left
infection, inflammation, leukemia
matured ones are called segs
what do you use a LAVANDER/PURPLE top for?
(2)
EDTA (anticoagulant)
CBC
what do you use a red or tiger red for?
seperates serum with centrifudge after sitting
blood banking/chemistries
what do you use a green top for?
heparnized tube, can be put on an analyzer faster than red
blood gases, chemistries, ice
what do you use a blue top for?
citrate (anticoagulant)
coagulation studies
**tube must be completely filled to validate or it throws the concentration off**
what do you use a gray top for?
(2)
glucose if delay to run is expected and lactate
what are three chemo drugs and what do they cause for irritation?
**think chemo man!!**
Doxorubicin (Adriamycin)- cardiac
bleomycin- pulmonary fibrosis!
cisplatin- renal dysfunction/oto toxic
basal cell carcinoma
what percent of melanoma is this? what does it look like? what 4 treatment options? what 2 preventions?
- 80% Basal cell *front pic*
(pearly nodule, telangectasias)
treatment: cut out, cryrosurgery, laser, Moh’s
prevention: fluorouracil, immunomodulators
melanoma
what are the 4 main types? where do you find them?
superficial spreading
lentigo maligna: sun exposure
acral lentiginous: palms, soles, nails, mucosa
nodular: deep pigmentation and deep invasion
***spreads by lymph and blood**
- breslow’s thickness: worse if >1mm tick, ulceration, mets*
- Clarks staging!! 1 (in situ)-5 (fat)*
TX: 2-4 wide excision “chunk of meat”, IFN, dicarbazine, cisplatin, vincristine
pleural effusion
what happens here? how do you diagnose this? what are the three treatment options for this?
intrathoracic fluid collection, dyspnea
DX: thoracentesis (diagnostic/palliative)
TX: sclerosis to prevent recurrance, insert chest tube, instill talc for pleurodesis (painful leads to scarring thus eliminating the space)
